Abstract
We examined the effects of the inhibitors of C1q or collagen biosynthesis. 2,2′-dipyridyl (DP), and 3,4-dehydro-DL-proline (DHP) on murine macrophage (Mφ) FcR subclass-mediated antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis of sheep erythrocyte targets. Oil-elicited peritoneal Mφ from C3HeB/FeJ mice which were cultured for 24 hr with DP (0.08 or 0.10 m M) or DHP (0.8 or 1.0 m M) showed a significant decrease in FcR subclass-mediated ADCC for murine monoclonal IgG 2a (FcRI) and IgG2b/IgG 1 (FcRII) as well as for heterologous polyclonal IgG. These collagen inhibitors also blocked phagocytosis mediated by both IgG 2a-and lgG 2b-opsonized erythrocytes. DP was more potent than DHP in blocking FcR effector functions in a reversible fashion and neither inhibitor affected Mφ C3b receptor function. Pretreatment of Mφ with collagenase resulted in significant reduction in FcR-mediated ADCC and phagocytosis. The inhibition of Mφ FcR subclass-mediated ADCC and phagocytosis by collagen C1q synthetic inhibitors or by collagenase treatment further confirms a functional relationship between cell-associated C1q and FcR-dependent functions.
Published Version
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